IVD of Bone Metabolism

Cat. #	Product name	Source (Host)	Species	Tag	Protein Length	Price
PTH-6070H	Recombinant Human PTH Protein (Ser32-Gln115), N-GST tagged	E.coli	Human	GST	Ser32-Gln115	Inquiry
PTH-6071H	Recombinant Human PTH Protein (Leu42-Gln115), N-His tagged	E.coli	Human	His	Leu42-Gln115	Inquiry
PTH-65H	Parathyroid Hormone, Human-Type, Synthetic (1-34) fragment Reference standard		Human	Non		Inquiry
PTH-66B	Parathyroid Hormone, Bovine-Type, Synthetic (1-34) fragment Reference standard		Bovine	Non		Inquiry
PTH-68B	Bovine Parathyroid Hormone Reference standard		Bovine	Non		Inquiry
PTH-P062H	Recombinant Human PTH therapeutic protein (Teriparatide)		Human	Non	34 Aa	Inquiry
Vitamin D-1001	Active Synthetic Vitamin D Protein, BSA conjugated	Synthetic		Non		Inquiry

What is Bone Metabolism?

Bone metabolism means the continual growth and destruction of bone tissue. It is a combination of the activity of osteoblasts (cells that make bones) and osteoclasts (cells that break down bones). This dynamic process is essential for the preservation, development and regeneration of the skeleton.

There are five primary aspects of bone metabolism:

1. Bone Formation: Osteoblasts generate new bone matrix and mineralize it, creating new bone tissue.
2. Bone Resorption: Osteoclasts dissolve the mineral structure of bone tissue, squander the organic structure and leak calcium and minerals into the bloodstream.
3. Regulation: Other hormones (such as PTH), vitamin D, calcitonin and sex hormones (estrogen and testosterone), mechanical stress and nutrition all regulate the functioning of bones.
4. Bone Remodeling: The constant replacement of deteriorated or aged bone with fresh bone material, thereby maintaining the integrity and stability of the bone.

The balance between bone formation and resorption is crucial to a healthy bone structure and density throughout life. This balance can be disrupted, for example, by bone disorders like osteoporosis, which leads to a reduction in bone mass and a greater tendency to fracture.

What is the most common metabolic bone disease?

The most prevalent metabolic bone disorder is osteoporosis. It's characterised by a loss of bone mass and density, resulting in increased fractures. Osteoporosis occurs when the growth of new bone doesn't keep up with the destruction of old bone, leaving the bones weakened and more likely to break. It also commonly occurs in adults who are older, and particularly postmenopausal women, because of hormonal changes.

What are the symptoms of metabolic bone disease?

The symptoms of metabolic bone diseases vary from condition to condition. But some common metabolic bone diseases symptoms include:

Bone Pain: The bone is experiencing chronic or permanent pain.
Fractures: Increased susceptibility to fractures, sometimes without significant trauma.
Deformities: Misshaped or abnormal bone structure.
Muscle Weakness: Reduced muscle strength and function.
Height Loss: A decrease in height over time, often associated with osteoporosis.
Stooped Posture: Gaining a hunched or stooped appearance, usually because of a spinal fracture.
Dental Problems: Teeth issues can occur in certain metabolic bone disorders.
Fatigue: Overall feeling of tiredness and lack of energy.
Reduced Mobility: Difficulty in walking or performing daily activities due to bone weakness.

What hormone is responsible for bone metabolism?

The primary hormone involved in bone metabolism is parathyroid hormone (PTH). PTH modulates the blood calcium level, alterations osteoclast activity (steepening bone resorption), and alters the production of vitamin D (a critical regulator of diet-induced calcium absorption). Other hormones, like calcitonin, and sex hormones (estrogen and testosterone), also affect bone metabolism.

How IVD use these protein/hormones?

Proteins and hormones such as parathyroid hormone (PTH), vitamin D, and bone turnover markers such as osteocalcin and bone-specific alkaline phosphatase serve as biomarkers in diagnosing and tracking diseases of the bone metabolism. We use IVD to detect the concentration and activity of these biomarkers in blood or urine to diagnose osteoporosis, Paget's disease, and other metabolic bone disorders.

Enzyme-Linked Immunosorbent Assay (ELISA):

Used widely to measure markers of bone turnover and hormones. Sensitive and specific for detecting proteins in blood samples.

Radioimmunoassay (RIA):

Monitors hormones like PTH and vitamin D. It requires radioactive labeling and is extremely sensitive.

Chemiluminescent Immunoassays:

Similar to ELISA but uses a chemiluminescent substrate. Allows for the detection and quantification of biomarkers with high sensitivity.

Mass Spectrometry:

Used for accurate quantification of vitamin D metabolites. Offers high specificity and precision.

Electrophoresis and Western Blotting:

Used to determine the levels and changes of specific proteins related to bone metabolism.

How do you treat bone metabolism?

Medications:

Bisphosphonates: Blocks the breakdown of bones and is widely used for osteoporosis.
Calcimimetics: For hyperparathyroidism to decrease parathyroid hormone levels.
Hormone Replacement Therapy (HRT): For post-menopausal women to maintain bone density.
Vitamin D and Calcium Supplements: To ensure proper bone health and metabolic functioning.

Lifestyle Modifications:

Dietary Changes: Ensure that you get the right amount of calcium and vitamin D.
Exercise: Physical activities to strengthen bones.
Avoiding Smoking and Excessive Alcohol: For a healthy bone.

Surgical Interventions:

In more severe cases, the need for surgery to correct bone deformities or fractures may be justified.

Management of Underlying Conditions:

Conditions such as hyperparathyroidism may be treated by a combination of prescription medication and surgery to destroy overactive thyroids.

Metabolic bone disease treatment typically depends on the type of illness and the patient. It's imperative to work closely with healthcare professionals to ensure that these disorders are optimally treated.

Advantages

High Purity
Batch Consistency
Scalability
Customizability
Ethical Production
Stability and Shelf-life
Functional Activity
Reduced Risk of Contamination

Case Study

Case 1: Bellorin-Font E, Rojas E, Martin KJ. Bone Disease in Chronic Kidney Disease and Kidney Transplant. Nutrients. 2022 Dec 29;15(1):167. doi: 10.3390/nu15010167. PMID: 36615824; PMCID: PMC9824497.

Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) comprises alterations in calcium, phosphorus, parathyroid hormone (PTH), Vitamin D, and fibroblast growth factor-23 (FGF-23) metabolism, abnormalities in bone turnover, mineralization, volume, linear growth or strength, and vascular calcification leading to an increase in bone fractures and vascular disease, which ultimately result in high morbidity and mortality.

Fig2. Examples of different types of bone disease in CKD Bone histology in CKD. (A) Panoramic view of normal bone histology. Magnification 4×. Toluidine blue staining. Figure shows interconnected bone trabeculae (purple). Clear areas between trabeculae represent medullary space. (B) Hyperparathyroid bone disease (high bone turnover). Magnification 20×. Goldner trichrome staining. Figure shows a resorption area with multinucleated osteoclast in the periphery. Area in blue corresponds to a calcified trabecula. (C) Adynamic bone disease (low bone turnover). Magnification 20×. Toluidine blue staining. Figure shows a bone section without cellular activity. Trabeculae are thin and disconnected. (D) Osteomalacia (low bone turnover). Magnification 20×. Toluidine blue staining. Figure shows abundant osteoid matrix (light blue) covering the mineralized bone trabecula. (E). Mixed uremic osteodystrophy (combines features of high turnover and osteoid matrix). Magnification 20×. Goldner trichrome staining.

Case 2: Wang LT, Chen LR, Chen KH. Hormone-Related and Drug-Induced Osteoporosis: A Cellular and Molecular Overview. Int J Mol Sci. 2023 Mar 18;24(6):5814. doi: 10.3390/ijms24065814. PMID: 36982891; PMCID: PMC10054048.

This review provides an overview of the cellular and molecular processes that drive bone turnover, the pathophysiology of osteoporosis and its treatment. RANCL seems to be the uncoupling factor responsible for osteoclastogenesis. Osteoprotegerin (OPG), by contrast, is a RANKL antagonist released from osteoblast lineage cells. Oestrogen kills osteoclasts and prevents osteoclastogenesis by promoting OPG production and suppressing osteoclast differentiation upon inhibition of IL-1 and TNF and subsequent M-CSF, RANKL and IL-6 release.

Fig3. A summary of the cellular and molecular mechanisms of bone turnover (osteoblasts, osteoclasts, osteocytes, mesenchymal stem cells [MSCs], and osteoclast precursors), the pathophysiology of hormone-related osteoporosis and drug-induced osteoporosis, and their treatment. Purple line: secrete; Orange line: increase/enhance; Blue line: decrease/inhibit; GC: Glucocorticoid; MSC: Mesenchymal Stem Cell.